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Peroxiredoxin 3 has important roles on arsenic trioxide induced apoptosis in human acute promyelocytic leukemia cell line via hyperoxidation of mitochondrial specific reactive oxygen species
- Title
- Peroxiredoxin 3 has important roles on arsenic trioxide induced apoptosis in human acute promyelocytic leukemia cell line via hyperoxidation of mitochondrial specific reactive oxygen species
- Authors
- Mun Y.-C.; Ahn J.Y.; Yoo E.S.; Lee K.E.; Nam E.M.; Huh J.; Woo H.A.; Rhee S.G.; Seong C.M.
- Ewha Authors
- 성주명; 유은선; 허정원; 이경은; 문영철; 남은미; 우현애
- SCOPUS Author ID
- 성주명; 유은선; 허정원; 이경은; 문영철; 남은미; 우현애
- Issue Date
- 2020
- Journal Title
- Molecules and Cells
- ISSN
- 1016-8478
- Citation
- Molecules and Cells vol. 43, no. 9, pp. 813 - 820
- Keywords
- Acute promyelocytic leukemia; Arsenic trioxide; Peroxiredoxin 3
- Publisher
- Korean Society for Molecular and Cellular Biology
- Indexed
- SCIE; SCOPUS; KCI
- Document Type
- Article
- Abstract
- NB4 cell, the human acute promyelocytic leukemia (APL) cell line, was treated with various concentrations of arsenic trioxide (ATO) to induce apoptosis, measured by staining with 7-amino-actinomycin D (7-AAD) by flow cytometry. 2’, 7’-dichlorodihydro-fluorescein-diacetate (DCF-DA) and MitoSOX™ Red mitochondrial superoxide indicator were used to detect intracellular and mitochondrial reactive oxygen species (ROS). The steady-state level of SO2 (Cysteine sulfinic acid, Cys–SO2 H) form for peroxiredoxin 3 (PRX3) was measured by a western blot. To evaluate the effect of sulfiredoxin 1 depletion, NB4 cells were transfected with small interfering RNA and analyzed for their influence on ROS, redox enzymes, and apoptosis. The mitochondrial ROS of NB4 cells significantly increased after ATO treatment. NB4 cell apoptosis after ATO treatment increased in a time-dependent manner. Increased SO2 form and dimeric PRX3 were observed as a hyperoxidation reaction in NB4 cells post-ATO treatment, in concordance with mitochondrial ROS accumulation. Sulfiredoxin 1 expression is downregulated by small interfering RNA transfection, which potentiated mitochondrial ROS generation and cell growth arrest in ATO-treated NB4 cells. Our results indicate that ATO-induced ROS generation in APL cell mitochondria is attributable to PRX3 hyperoxidation as well as dimerized PRX3 accumulation, subsequently triggering apoptosis. The downregulation of sulfiredoxin 1 could amplify apoptosis in ATO-treated APL cells. © The Korean Society for Molecular and Cellular Biology. All rights reserved.
- DOI
- 10.14348/molcells.2020.2234
- Appears in Collections:
- 의과대학 > 의학과 > Journal papers
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